The analysis of data on the prevalence of hypothyroidism in areas
with different concentrations of fluoride in the public drinking water
supplies, by workers at the University of Kent,[1] is interesting but by
no means conclusive. The authors rightly emphasise that their findings do
not prove that fluoridation causes people to develop the condition,but
only that there is a clear correlation. In fact this study raises m...
The analysis of data on the prevalence of hypothyroidism in areas
with different concentrations of fluoride in the public drinking water
supplies, by workers at the University of Kent,[1] is interesting but by
no means conclusive. The authors rightly emphasise that their findings do
not prove that fluoridation causes people to develop the condition,but
only that there is a clear correlation. In fact this study raises more
questions that it actually answers.
Public Health England's Water Fluoridation Health Monitoring Report
for England 2014 [2], so widely cited by supporters of the practice, is in
fact riddled with statistical improprieties. It has become the norm for
the dental public health sector to dismiss all complaints that
fluoridation is harmful to thyroid function, and the 2014 PHE report fails
to mention it at all. This study appears to challenge that position.
In this new study the authors report that there is an at least 30%
greater prevalence of hypothyroidism in areas with more than 0.3mg/l of
fluoride in the public water supplies. However, this limit is not a
threshold; it is merely the dividing point between two out of the three
arbitrarily chosen ranges of fluoride concentration in drinking water. The
apparent 'boundary' between a safe and an unsafe concentration of fluoride
is an experimental artifact, not a representation of what happens in real
life.
So it is only permissible to draw a generalised conclusion from this
study. This is disappointing. Fluoride overdose is now endemic - half of
all children growing up in fluoridated water areas develop at least some
detectable form of dental fluorosis, the only visible biomarker for
incipient fluoride toxicosis. In non-fluoridated areas the prevalence of
this condition is around one quarter.
Clearly, other sources of bioavailable fluoride are already
contributing to this undesirable body-burden. If there is a causative link
between fluoride absorption and thyroid function, then it is reasonable to
propose that all bioavailable fluoride sources may contribute to the
problem. This would imply that that many people may be prone to
hypothyroidism due to the increasing background contamination of our foods
and dental products with fluoride. If so, this might suggest that the
extra fluoride in some water supplies may be pushing more people over the
threshold at which GPs start to notice that more of their patients have
this condition.
Another missed opportunity?
There is one intriguing feature of this study that illustrates what
could be done to clarify our understanding of the medical consequences of
water fluoridation, if only the government would stop prevaricating and
put some real effort into sorting out the whole mess.
This new study compares hypothyroidism prevalence across the country
with data on the average annual fluoride level maintained in drinking
water supplies during 2012. Those of us in the Lake District will be aware
that, although the authors show (correctly) that West Cumbria was not
fluoridated in 2012, in fact the region has been fluoridated since around
1970.
The local water supplier, United Utilities, shut down its
fluoridation activities in 2007 to carry out maintenance, resuming
fluoridation in September 2013. So for six years those people who had been
drinking fully fluoridated water for up to almost forty years had their
access to the 'benefits' of this product interrupted.
Both accidents and anomalies can provide unique opportunities to
examine novel questions that that may never be considered when looking at
generalised data, and this six year halt to fluoridation in West Cumbria
provided just such an opportunity. So it is unfortunatle that the new
study does not reveal whether the risk of hypothyroidism in West Combria
is elevated.
It would have been enormously interesting to learn how prevalent
hypothyroidism was in this area before and during, and is now after, that
fluoride-free interlude. Was the prevalence of the condition elevated
before fluoridation stopped? If so, did it fall, during the hiatus in
supply? And has it increased again since?
Presumably raw data are available to answer these questions, but have
not yet been analysed. It would be fascinating to see whether or not the
prevalence of hypothyroidism changed. The results of such an analysis
might yet provide support for proposing that correlation may reasonably
imply causation and, if so, whether stopping the practice in other
fluoridated areas might bring similar relief to the afflicted.
Douglas Cross, CSci, CBiol. FSB.
References
1. Peckham S, Lowery D, Spencer S.(2015) Are fluoride levels in
drinking water associated with hypothyroidism prevalence in England? A
large observational study of GP practice data and fluoride levels in
drinking water. J Epidemiol Community Health 2015;0:1-6.
doi:10.1136/jech-2014-204971
2. Public Health England. Water Fluoridation. Health monitoring
report for England
2014. PHE publications gateway number: 2013547, 2014.
In relation to the reported findings in this study of a correlation
between higher socioeconomic position and incidence of brain tumour,
specifically giloma and acoustic neuroma, among a cohort of Swedish-born
residents, the authors postulate 'completeness of cancer registration' and
'detection bias' as a potential explanation.
This seems unlikely, especially given the progressive nature of brain
tumour pathology...
In relation to the reported findings in this study of a correlation
between higher socioeconomic position and incidence of brain tumour,
specifically giloma and acoustic neuroma, among a cohort of Swedish-born
residents, the authors postulate 'completeness of cancer registration' and
'detection bias' as a potential explanation.
This seems unlikely, especially given the progressive nature of brain
tumour pathology, i.e. socioeconomic background would have little effect
on the eventual likelihood of a patient entering the (taxpayer funded)
medical system, and thus small statistical significance.
In May 2011, the International Agency for Research on Cancer
classified radiofrequency electromagnetic fields - as emitted by mobile
phones - as "possibly carcinogenic to humans" (IARC Group 2B), based on
"limited" epidemiological studies showing an indication of an increased
risk of glioma or acoustic neuroma.
In May 2016, it was reported (http://microwavenews.com/news-
center/ntp-cancer-results) that the US government's recently completed $25
million National Toxicology Program study shows statistically significant
increases in cancer - specifically giloma and malignant schwannoma of the
heart, the latter affecting the same type of cell as acoustic neuroma -
among rats that had been exposed to GSM or CDMA signals for two years.
Is it not the case that those with higher SEP, i.e. professionals as
opposed to manual labourers, would statistically be more likely to have an
increased exposure to microwaves from both cordless and mobile phones,
used as an administrative tool in the workplace (regardless of personal
use outside of these hours).
Mobile phone use in the workplace became widespread during the 1980's
and onwards. The authors of this study looked at a primary diagnosis of
brain tumour among cohort members between 1993 and 2010. Allowing for a
latency period of up to 10 years plus for the development of brain tumour
following carcinogenic exposure, is it not worth exploring this potential
link, rather than the somewhat weaker theory of 'detection bias'.
Sir,
We have read with particular interest the paper by Wu C. et al. on the association of retirement age with mortality among older adults in a large US study.[1] We need deeper understanding of the association found between a 1-year age increment in the 2,956 participants and an 11% lower risk of all-cause mortality (95% confidence interval 8-15%). The authors conclude that "early retirement may be a risk factor for mortality a...
Sir,
We have read with particular interest the paper by Wu C. et al. on the association of retirement age with mortality among older adults in a large US study.[1] We need deeper understanding of the association found between a 1-year age increment in the 2,956 participants and an 11% lower risk of all-cause mortality (95% confidence interval 8-15%). The authors conclude that "early retirement may be a risk factor for mortality and prolonged working life may provide survival benefits". It is true that employment is a major component of individual identity, as the authors' state. However, the discussion about reverse causality needs further development, since working conditions might partly explain these results: poor working conditions are related to shorter employment spans, and also to poorer health, while ending work with retirement is associated with a positive lifestyle and health changes.[2,3]. Thus in analyzing the relation between early retirement and mortality the authors should more deeply explore working conditions, including physical and psychosocial exposures during the working life, known to have long-term effects on health.[4,5] The division of occupations into three categories (white collar, blue collar, service, not even included in the final model) is too crude for comparing positive and negative working environments. Using working characteristics, job-exposure matrices, or proxy measures, might be considered for this, if available.
In conclusion, we agree with the authors on the possible positive effect of prolonged working life, but the effects of working conditions should be considered, detailed, and discussed.
Acknowledgements
We would like to thank Richard Carter for helping us to improve the language of this document.
References
1 Wu C, Odden MC, Fisher GG, et al. Association of retirement age with mortality: a population-based longitudinal study among older adults in the USA. J Epidemiol Community Health Published Online First: 21 March 2016. doi:10.1136/jech-2015-207097
2 Westerlund H, Vahtera J, Ferrie JE, et al. Effect of retirement on major chronic conditions and fatigue: French GAZEL occupational cohort study. BMJ 2010;341:c6149.
3 Ding D, Grunseit AC, Chau JY, et al. Retirement-A Transition to a Healthier Lifestyle?: Evidence From a Large Australian Study. Am J Prev Med Published Online First: 8 March 2016. doi:10.1016/j.amepre.2016.01.019
4 Descatha A, Herquelot E, Carton M, et al. Is physically arduous work associated with limitations after retirement? Findings from the GAZEL cohort. Occup Environ Med 2016;73:183-6. doi:10.1136/oemed-2015-103130
5 D'Angelo S, Coggon D, Harris EC, et al. Job dissatisfaction and the older worker: baseline findings from the Health and Employment After Fifty study. Occup Environ Med Published Online First: 5 May 2016. doi:10.1136/oemed-2016-103591
Conflict of Interest:
No conflict of Interest. Authors received fees from their institutions for their work (Paris hospital and Versailles University). Thomas Despreaux and Alexis Descatha have no relevant conflict of interest. Alexis Descatha has received fees from Elsevier Masson as editor-in-chief of the journal "les archives des maladies professionnelles et de l'environnement".
We commend the authors for taking the hypothesis that cancer may have
its roots in early life social conditions seriously [1]. Social
inequalities exist for many cancer types and are usually attributed to
differences in lifestyles and behaviours. Thus, attempts at primary
prevention are often confined to relatively proximal disease risk factors
at the individual level.
We commend the authors for taking the hypothesis that cancer may have
its roots in early life social conditions seriously [1]. Social
inequalities exist for many cancer types and are usually attributed to
differences in lifestyles and behaviours. Thus, attempts at primary
prevention are often confined to relatively proximal disease risk factors
at the individual level.
Cancer development has mainly been considered as a consequence of DNA
mutations and consequently tends to be viewed through the lens of
molecular biology. However, cancer may be a disease model particularly
relevant to investigate how the social becomes biological, via a
lifecourse approach. Many socially stratified biological mechanisms have
been identified as being part of the causal chain of risk for cancers:
material exposures (including inert ones such as asbestos, or living ones
such as the Helicobacter pylori virus) and behavioural mechanisms
(including tobacco consumption and fatty food intake). Furthermore, the
lifecourse approach is of particular interest when studying cancer because
of the long latent time period during which exposures occur, before the
onset of disease. There is increasing evidence for the role of chronic
stress from early life in cancer development and progression.
Upstream, cancer aetiologies differ, some being exogenous in origin
(viruses, smoking) and others endogenous (hormonal cancers). However all
cancers are at some point rooted in the immune and inflammatory system,
and thereby their initiation is susceptible to factors affecting
biological mechanisms at some point along this aetiological pathway. If
the immune system is impaired from killing-off damaged cells, the risk of
developing tumour cells is heightened [2]. A damaged immune system is also
an important accelerator of cancer progression [3]. This root in the
immune system is currently the source of the most promising immune-therapy
treatment for many cancers [4]. In fact, there is increasing evidence that
chronic stress may influence immune and inflammatory systems, implicating
socially driven epigenetic mechanisms, which may represent an overall set
of early life social determinants of cancer development over the
lifecourse [5]
Evidence on the link between early life stress and cancer in
epidemiology remains sparse and inconclusive, and presents difficult
methodological issues. Measuring early life physiological stress remains a
challenge, but one worth investing in since acute versus chronic stress,
and the timing of stress in early life may be important for subsequent
stress responses. Stressful events are likely to be experienced
differently depending on an individual's hierarchical position on the
social gradient. Individuals lower on the social gradient may be more
vulnerable to the physiological or behavioural effects of stressful
environmental exposures with fewer resources and buffering strategies at
their disposal compared to individuals with a higher social position [6].
Social gradients may also confer stress to individuals via status anxiety,
which has also been shown in non-human primates [7]. Intra-familial
conditions occurring from conception into adolescence may program
physiological responses during sensitive periods of development, altering
an individual's biology, rendering them susceptible when faced with
exposures later in life [8]. We hypothesize that taking into account
socially driven early life exposures to chronic stress is important to
understanding the aetiology of cancers, which have a common root in the
immune and inflammatory systems. These systems form part of the overall
physiological stress response.
We have inadequately attempted to examine this hypothesis, showing
that early life adversity and social position is associated with adult
cancers before the age of 50 [9]. However, due to a gaping hole in the
available lifecourse data combined with good quality cancer incidence data
in adulthood, the hypothesis remains to be fully investigated. As well as
having mortality data, cancer incidence data provided by registries would
allow for a better understanding of cancer aetiological pathways from
early life social conditions onwards, and potentially highlight new areas
for the primary prevention of cancers. We agree with the authors' point
about investing resources into data, and we would emphasise the need for
quality data on cancer incidence specifically. To truly get to grips with
the aetiology of cancers, concerted investment in the birth cohort
studies, and their linkage with registries is paramount.
1 Vohra J, Marmot MG, Bauld L, et al. Socioeconomic position in
childhood and cancer in adulthood: a rapid-review. J Epidemiol Community
Health 2016;70:629-34.
2 Stewart TJ, Abrams SI. How tumours escape mass destruction. Oncogene
2008;27:5894-903.
3 Kim R, Emi M, Tanabe K. Cancer immunoediting from immune surveillance to
immune escape. Immunology 2007;121:1-14.
4 Dustin ML. Cancer immunotherapy: Killers on sterols. Nature 2016;531:583
-4.
5 Kelly-Irving M, Mabile L, Grosclaude P, et al. The embodiment of adverse
childhood experiences and cancer development: potential biological
mechanisms and pathways across the life course. International Journal of
Public Health 2013;58:3-11.
6 Baum A, Garofalo JP, Yali AM. Socioeconomic Status and Chronic Stress:
Does Stress Account for SES Effects on Health? Ann N Y Acad Sci
1999;896:131-44.
7 Sapolsky RM. The Influence of Social Hierarchy on Primate Health.
Science 2005;308:648-52.
8 Bailey DBJ, Bruer JT, Symons FJ, et al., eds. Critical thinling about
critical periods. Baltimore: Paul H. Brookes publishing co. 2001.
9 Kelly-Irving M, Lepage B, Dedieu D, et al. Childhood adversity as a risk
for cancer: findings from the 1958 British birth cohort study. BMC Public
Health 2013;13:767.
Droomers et al. examined the association between green space
interventions in Dutch deprived neighborhoods and short-term impacts on
physical activity (PA) and perceived general health (PGH) among adults.
The authors reported an absence of short-term positive effects on PA and
health from improvements in green space in deprived neighbourhoods.[1]
The authors made significant efforts to control for the clusterin...
Droomers et al. examined the association between green space
interventions in Dutch deprived neighborhoods and short-term impacts on
physical activity (PA) and perceived general health (PGH) among adults.
The authors reported an absence of short-term positive effects on PA and
health from improvements in green space in deprived neighbourhoods.[1]
The authors made significant efforts to control for the clustering of
individuals within neighbourhoods and to adjust analyses at both
individual and neighbourhood levels.[1] They acknowledged several
shortcomings in the research design including the wide range of
socioeconomic interventions undertaken by the Dutch District Approach, in
addition to the varied mix of locally tailored green space
interventions.[1, 2] However, effect modifiers and information bias were
possibly introduced in the study design leading to inaccurate conclusions.
Social neighbourhood environments are considered to be effect
modifiers.[3, 4] However, the overall intensity of the Dutch District
Approach method used to adjust for the impact of interventions not related
to green space was based on the number of interventions;[1] not on the
type of interventions. Therefore, a fully justified sample size allowing
stratified analysis was needed.
Furthermore, I argue that exposure and outcome measures possibly
introduced information bias limiting opportunities to capture positive
impacts of green space interventions on PA and health. Information about
respondents' use of green space is vital to examine their impacts on PA
and health.[2, 4] However, green space exposure was not measured in terms
of use, access or proximity to green space interventions, but in terms of
their implementation. This information bias might have pulled the results
toward the null hypothesis, as the assumption was that all respondents
were "exposed" to green space interventions, but this was not necessarily
true. Differential misclassification of outcomes was also potentially
introduced. Given the variety of green space interventions (e.g. community
gardens), PA domains specifically related to these green space
interventions might have shed light on the impact of the neighbourhood
green space attributes.[4] In addition to PGH, the study would have been
more robust if physical, mental, and social health constructs had been
operationalized.[5]
Doomers et al. reported that green space interventions do not impact
PA and health. Given the wide variety of interventions: 1) a fully
justified sample size allowing stratified analysis and 2) measures, which
accurately classify exposure to green space and capture PA and health
domains specifically related to green space interventions are needed to
limit potential type II error.
References
1 Droomers M, Jongeneel-Grimen B, Kramer D, et al. The impact of
intervening in green space in Dutch deprived neighbourhoods on physical
activity and general health: results from the quasi-experimental URBAN40
study. J Epidemiol Community Health 2016;70:147-154. doi:10.1136/jech-2014
-205210
2 Droomer M, Harting J, Jongeneel-Grimen B, et al. Area-based
interventions to ameliorate deprived Dutch neighborhoods in practice: Does
the Dutch District Approach address the social determinants of health to
such an extent that future health impacts may be expected? Prev Med
2014;61:122-127. http://dx.doi.org.qe2a-
proxy.mun.ca/10.1016/j.ypmed.2014.01.009
3 Diez Roux AV, Mair C. Neighborhoods and health. Ann NY Acad Sci
2010;1186:125-145. doi: 10.1111/j.1749-6632.2009.05333.x
4 Hunter RF, Christian H, Veitch J, et al. The impact of
interventions to promote physical activity in urban green space: A
systematic review and recommendations for future research. Soc Sci &
Med 2015;124:246-256. http://dx.doi.org.qe2a-
proxy.mun.ca/10.1016/j.soscimed.2014.11.051
5 van den Berg AE, Maas J, Verheij RA, et al. Green space as a buffer
between stressful life events and health. Soc Sci & Med 2010;70:1203-
1210. doi:10.1016/j.socscimed.2010.01.002
Ribeiro and colleagues' identify high mortality rates at older ages
in the post-industrial UK areas of Merseyside and West Central Scotland
(WCS). They suggest that poverty and a lack of social cohesion may be part
of the explanation for this finding (1). Merseyside and WCS are
characterised by wide intra-regional variation in mortality rates compared
to other deindustrialised areas across Europe, possibly reflecting grea...
Ribeiro and colleagues' identify high mortality rates at older ages
in the post-industrial UK areas of Merseyside and West Central Scotland
(WCS). They suggest that poverty and a lack of social cohesion may be part
of the explanation for this finding (1). Merseyside and WCS are
characterised by wide intra-regional variation in mortality rates compared
to other deindustrialised areas across Europe, possibly reflecting greater
inequalities (2).
Although these areas are relatively deprived in a UK context, they
are not so in European context and the substantially higher mortality in
WCS compared to Merseyside is not explained by poverty. Glasgow's
mortality remains higher than expected, when compared to Liverpool, even
taking into account its relative age, sex and deprivation profile - a
phenomenon known as Glasgow's 'excess mortality'(3). Thus, there is more
to the explanation of health differences between these post-industrial
areas than poverty alone.
Levels of social cohesion have been suggested as a potential contributory
cause for this 'excess mortality' (3). A survey of Glasgow, Liverpool and
Manchester, found that the population of Liverpool had substantially
higher social cohesion (e.g. trust and reciprocity) than Glasgow, despite
almost identical poverty and deprivation levels (4). Research is underway
to understand why the social fabric of Liverpool differs from Glasgow, and
in particular the role of historical regional and urban policy in
fostering (e.g. through popular political activity) or damaging (e.g.
through the diversion of investment away from the city) this.
The findings of Ribeiro and colleagues point to an important
mortality phenomenon, but caution should be exercised before we explain
these findings without due attention to historical and political context.
1. Ribeiro AI, Krainski ET, Carvalho MS, de F?tima de Pina M. Where
do people live longer and shorter lives? An ecological study of old-age
survival across 4404 small areas from 18 European countries. Journal of
Epidemiology and Community Health. 2016.
2. Taulbut M., Walsh D., McCartney G., Parcell S., Hartmann A., Poirier
G., et al. Spatial inequalities in life expectancy within post-industrial
regions of Europe. BMJ. 2014;4(6).
3. McCartney G, Collins. C, Walsh D, Batty D. Accounting for Scotland's
Excess Mortality: Towards a Synthesis Glasgow Centre for Population
Health, 2011.
4. Walsh D, Gerry McCartney, Sarah McCullough, Marjon van der Pol, Duncan
Buchanan, Jones R. Exploring potential reasons for Glasgow's 'excess'
mortality: Results of a three-city survey of Glasgow, Liverpool and
Manchester. Glasgow Centre for Population Health, NHS Health Scotland and
the University of Aberdeen, 2013.
Recent review from Harris et al [1] sets the alternative hypothesis
that greater degree of stakeholders participation can produce a
contextually valid synthesis. Aware of the importance of stakeholders in
healthcare, a null hypothesis may come to mind: Stakeholders increase
inequity by biasing synthesis. Let us give you some theoretical framework.
Research on public health interventions should include academic
researcher...
Recent review from Harris et al [1] sets the alternative hypothesis
that greater degree of stakeholders participation can produce a
contextually valid synthesis. Aware of the importance of stakeholders in
healthcare, a null hypothesis may come to mind: Stakeholders increase
inequity by biasing synthesis. Let us give you some theoretical framework.
Research on public health interventions should include academic
researchers and local stakeholders to ensure that results are relevant to,
and useful for, decision-makers. The idea is that stakeholders involvement
also increases transparency and truthfulness of research process [2].
Thus, the partnership "researcher-stakeholder" may be successful in
improving health outcomes.
Given its goal, the scope of stakeholders involvement is wide, including
patients, caregivers, clinicians, researchers, advocacy groups,
professional societies, businesses, policymakers, or others. These people
that emerge from general population are also vulnerable to health
inequalities. Then, what if there is a gap, within stakeholder, between
the most and the least disadvantaged? This scenario can lead to biased
results because of two reasons: 1) Marginalization of vulnerable
populations that are valuable for the researcher-stakeholder partnership,
and 2) Unfairness selection of stakeholders that reproduces inequality in
a particular way by allowing some people to mobilize capital for their own
benefit, blending self-interest and public interest which is a difficult
enterprise [3].
Allowing some individuals to have greater probability of become
stakeholder could, as I already mention, produce biased results. Biased
results leads to wrong decision-making and to interventions that initially
benefit only those with higher socio-economic status and therefore
inadvertently increase inequities, a situation called "the inverse equity
hypothesis" [4]
Thus, one can easily conclude one big issue in the role of stakeholders in
research: we must assure significant inclusion of the most disadvantaged.
How? Using proper procedures for obtaining persons from the target
population to build the stakeholder team.
Finally, based on this short dissertation a question emerges to pose to
Dr. Harris: Did you use special procedures to assure a significant
inclusion of individuals to stakeholder team? In other words: do you think
is important to consider selection bias when setting up the stakeholder
team?
Acknowledgments: Victor C. Kok MD. PhD. Asia University
Conflict of interest: No one to declare.
References:
1 Harris J, Croot L, Thompson J, et al. How stakeholder
participation can contribute to systematic reviews of complex
interventions: Figure 1. J Epidemiol Community Health 2015;70:jech - 2015-
205701. doi:10.1136/jech-2015-205701
2 AHRQ. Stakeholder Guide 2014. Stakehold Guid 2014 2014;:15-
6.http://www.ahrq.gov/research/findings/evidence-based-
reports/stakeholderguide/stakeholdr.pdf
3 Klenk NL, Meehan K, Pinel SL, et al. GLOBAL CHANGE SCIENCE.
Stakeholders in climate science: Beyond lip service? Science 2015;350:743-
4. doi:10.1126/science.aab1495
4 Victora CG, Vaughan JP, Barros FC, et al. Explaining trends in
inequities: evidence from Brazilian child health studies. Lancet (London,
England) 2000;356:1093-8. doi:10.1016/S0140-6736(00)02741-0
Hehir (2015) gives an interesting account on the current trends in
breech delivery and gives discusses several large studies whose findings
suggest that differences in mortality between vaginal breech delivery and
elective cesarean section are minimal. Considering the down sides of
cesarean delivery, such as increased risks during future pregnancies and
births, what is the best option for women? And who should make that...
Hehir (2015) gives an interesting account on the current trends in
breech delivery and gives discusses several large studies whose findings
suggest that differences in mortality between vaginal breech delivery and
elective cesarean section are minimal. Considering the down sides of
cesarean delivery, such as increased risks during future pregnancies and
births, what is the best option for women? And who should make that
decision?
Vaginal breech delivery rates are decreasing, with more obstetricians
opting for cesarean delivery and some even using a 'no- option' approach
when it comes to vaginal breech delivery (Hehir, 2015). This 'no-option'
approach means that women are not given the chance to make informed
decisions about their own healthcare- a principle which is fundamental to
current medical practice (Dyer, 2015). Of course there are challenges, and
the fast pace and anxiety provoking environment of an emergency breech
delivery is not the ideal situation to be making these decisions. It is
therefore important that women are given information about their options
early on in their pregnancy so that a plan can be agreed between the
patient and the rest of the medical team.
References
Dyer. C. 2015. Doctors should not cherry pick what information to give to
patients, court rules. British Medical Journal. 350.
Hehir. M. 2015. Trends in Vaginal Breech Delivery. Journal of
epidemiology and Community Health. 69:12.
It appears somewhat bizarre that authorities have ignored a widely
consumed source of fluoride from tea although insisting on community water
fluoridation (CWF) to reduce dental decay. Notably, black tea in
commercial teabags contains significant levels of fluoride. This is
especially so when sourced from Kenya with volcanic soils compounded by
fluoride from superphosphate fertilisers. Mechanical harvesting then
includes...
It appears somewhat bizarre that authorities have ignored a widely
consumed source of fluoride from tea although insisting on community water
fluoridation (CWF) to reduce dental decay. Notably, black tea in
commercial teabags contains significant levels of fluoride. This is
especially so when sourced from Kenya with volcanic soils compounded by
fluoride from superphosphate fertilisers. Mechanical harvesting then
includes older leaves with higher fluoride content than the young hand-
picked tips.
Habitual tea drinkers with a daily consumption of 3 cups of tea could
already be obtaining more than adequate or safe fluoride intake based on
the WHO (2002) upper limit recommendations of 2mg/day for children and 4mg
for adults.
Peckham's multicentre GP study revealing 30% higher hypothyroidism in
areas where the water supply exceeded 0.3ppm of fluoride must raise
serious questions regarding HFSA toxicity as nationwide, the British are
traditionally tea drinkers. Thus all areas would already be getting
fluoride from tea yet only those with CWF had increased hypothyroidism
rates.
Oksuzyan et al. report an association between race/ethnicity and two
subtypes of childhood leukemia: acute lymphoblastic leukaemia (ALL) and
acute myeloid leukaemia (AML).1 Accordingly, the researchers suggest that
there are genetic, cultural, and environmental factors involved in the
etiology of childhood leukaemia [1].
Importantly, Oksuzyan et al. made a significant effort to examine and
control for the poten...
Oksuzyan et al. report an association between race/ethnicity and two
subtypes of childhood leukemia: acute lymphoblastic leukaemia (ALL) and
acute myeloid leukaemia (AML).1 Accordingly, the researchers suggest that
there are genetic, cultural, and environmental factors involved in the
etiology of childhood leukaemia [1].
Importantly, Oksuzyan et al. made a significant effort to examine and
control for the potential role of socioeconomic status (SES) on this
association. In particular, the authors used paternal education levels
used as a proxy for SES given that a significant percentage of information
on maternal education was missing from the birth registry used [1]. This
strategy faces several challenges given the complex association of race,
education, and SES.
The use of paternal education might not appropriately account for the
adverse health effects which might result (at least in part) from residing
in single-parent homes. It has been widely documented that children
frequently exhibit poor health outcomes in single-parent homes due to
causal chain of effects related to parent's education, SES, and income
[2]. Moreover, the information regarding paternal education as a proxy for
SES was obtained from the California Birth Registry [1]. It is possible
that this data does not adequately represent the SES of the cases used in
the study given that the father identified might not have provided
financial support for the child.
In addition, the use of parental education as a proxy for SES may not
be an appropriate method as average income frequently varies in jobs
requiring similar education levels [3]. It is possible that these
variations occur more frequently among different ethnic/racial groups;
potentially as a result of systemic prejudice and/or unequal employment
opportunities [3].
Oksuzyan et al. report an association between race/ethnicity and
childhood leukaemia [1]. Due to potential challenges in using paternal
education as a proxy for SES, the inclusion of maternal education and a
discussion regarding SES in single-parent homes would have been valuable.
References
1 Oksuzyan S, Crespi CM, Cockburn M, Mezei G, Vergara X, Kheifets L.
Race/ethnicity and the risk of childhood leukaemia: A case-control study
in California. J Epidemiol Community Health Published Online First: 19
March 2015. doi:10.1136/jech-2014-204975
2 Gucciardi E, Celasun N, Stewart DE. Single-mother families in
Canada. Can J Public Health 2004;95(1):70-73.
3 Williams DR. Race, socioeconomic status, and health. The added
effects of racism and discrimination. Ann N Y Acad Sci 1999;896:173-188.
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